Yuguo Yu, Yousheng Shu, and David A. McCormick
Axon potentials recorded in somata of pyramidal neurons in vivo have a libertine rising form and variable threshold, contrary to predictions of the Hodgkin�CHuxley simulation. Some have suggested that this difference is due to cooperativity among atomic number 11 channels, resulting in many channels opening simultaneously. Yu et al. now show that the shape and threshold variance of somatic action potentials can be explained by the fact that spikes backpropagate to the frame from their initiation point, ~40 ��m along the axon. Simultaneous intracellular recordings from somata and axons in cortical slices revealed that the shape and threshold unevenness of spikes at the spike-initiating zone were logical with predictions of the Hodgkin�CHuxley framework. Computer simulations confirmed that the resurrect times of spikes in the sarcostemma acidum were influenced by backpropagation, and that threshold unevenness resulted from differences in membrane potential in the soma and axon initial segment at the time of spike initiation.
2. SCLIP Role in Purkinje Cell Dendritogenesis
Fabienne E. Poulain, St�phanie Chauvin, Rosine Wehrl� Mathieu Desclaux, Jacques Mallet, Guilan Vodjdani, Isabelle Dusart, and Andr� Sobel
Purkinje cells develop highly forked dendritic arbors that get tens of thousands of synaptic inputs. Poulain et al. reputation this week that SCLIP, a member of the stathmin household of microtubuledestabilizing proteins, is important in Purkinje cadre dendritogenesis. In the developing cerebellum, SCLIP was explicit primarily in Purkinje cells, became saturated in dendrites as they formed, and decreased when the dendritic arbor was fully formed. The expression was concentrated in the Golgi setup and other vesicular structures. Overexpression of SCLIP in postnatal organotypic cerebellar cultures accelerated dendritic development and increased the number and branching of primary dendrites. Conversely, early knockdown of SCLIP via RNA suppression inhibited the initial formation of dendrites, and subsequently knockdown inhibited growth and branching of nascent dendrites. Importantly, contiguous Purkinje cells that were not transfected with meddling RNAs highly-developed normally, indicating that SCLIP affects dendritogenesis only in the cadre in which it is expressed.
3. Stress and Cannabinoids
Silvia Rossi, Valentina De Chiara, Alessandra Musella, Hajime Kusayanagi, Giorgia Mataluni, Giorgio Bernardi, Alessandro Usiello, and Diego Centonze
The human relationship between tension and the endocannabinoid scheme are building complex, and energizing of cannabinoid receptors tin can have divers and apparently contradictory personal effects on the stress response. This complexity is further demonstrated this week by Rossi et al., world Health Organization show that stress has different effects on GABAergic and glutamatergic transmission in the striatum, a brain area that has heights levels of cannabinoid receptors and is important in stress responses. Mice were subjected everyday to an aggressive male to hasten social stress, and the effects of exogenous and endogenous cannabinoids were measured in corticostriatal slice cultures. Stress exposure eliminated the reductions in GABAergic IPSC frequency and amplitude that are normally produced by cannabinoids. In contrast, stress did non alter cannabinoid-mediated reduction in glutamatergic EPSC frequency and amplitude. Providing mice with rewards (exercise, sugar, or cocaine) subsequently social stress eliminated the effects of stress on cannabinoid modulation of GABAergic transmission.
4. Voltage-Gated Sodium Channel Mutations in Migraine
Sandrine Cest��le, Paolo Scalmani, Raffaella Rusconi, Benedetta Terragni, Silvana Franceschetti, and Massimo Mantegazza
Different mutations in the neuronal voltage-gated sodium channel (Nav1.1) drive familial hemiplegic migraine (FHM) or epilepsy. To assist differentiate the physiological bases of these diseases, Cest��le et al. expressed human Nav1.1 channels bearing the FHM case 3 mutation (which results in an amino acid substitution in the inactivation gate) in a non-neural cell line and in cultured neocortical neurons. The electrophysiological properties of the mutant line were consistent with it conferring a limited hyperexcitability on neurons. Compared to wild type, mutated channels had a positive shift in the voltage habituation of deactivation, reduced upper limit current denseness, and quicker inactivation. Some of these properties are expected to produce hyperexcitability, and others should party favor hypoexcitability. Mutant channels appeared able to sustain high frequency firing better than wild-type channels, only this ability was limited and disappeared after sustained depolarization. This limited hyperexcitability may tell migraine and epilepsy mutations.
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Source: Sara Harris
Society for Neuroscience
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